Changes in Plasma Nitrate Levels in the Acute Phase of Kawasaki Disease

Abstract

Aim: Plasma nitrate, the stable end product of nitric oxide(NO), has been reported as an indirect measure of the whole body NO production. The purpose of this study is to measure plasma nitrate in the acute phase of Kawasaki disease, and to evaluate NO pr oduction in patients with and without coronary artery lesions. Methods: Thirty patients aged 3 months to 6 years were enrolled in this study. Blood samples were obtained serially on the 1, 2, 3, 4, and 8th week of illness. Plasma nitrate was measured by h igh-performance liquid chromatography. Twenty-six patients were treated with aspirin (10-30mg/kg/day) and intravenous immunoglobulin (2g/kg single dose). Four patients received only aspirin. Results: We classified the subjects into 3 groups: normal coro nary artery (group N, n=15), coronary dilatation and aneurysm(group D, n=9), transient coronary dilatation (group T, n=6). In all groups, plasma nitrate increased significantly from the 1st week to the 2nd week (p<0.05). Peak levels of nitrate (mean+ mn;SEM, μmol/L) in each group were as follows: group N=73.0±15.8, group D=52.3±12.9, group T=58.5±4.4, respectively. Plasma nitrate fell from the 3rd week to the 4th and 8th weeks, but still elevated in each group in compariso n with age-matched healthy controls (22.1±8.8): group N=50.9±5.3, group D=46.8±9.3, group T=29.0±1.8. There were no correlations between plasma nitrates and C-reactive protein, neutrophil counts and the Harada score, respective l y. Conclusion: Increased production of NO in the first 2nd to 3rd weeks of the acute phase was observed. It was consistent with the pathological stage of generalized microvasculitis and myocarditis. Plasma nitrates in group D were lower than those in gr oup N through the course of 8 weeks, indicating decreased NO production due to impairment of the endothelial function.